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Tissue-resident memory T (TRM) cells have been studied mainly in mouse models. Schumacher and colleagues have developed an imaging technology to track in real time skin-resident human CD8+ TRM cells in situ.

Nephritis is a major cause of lupus morbidity. Putterman and colleagues use single-cell RNA sequencing on human renal and skin biopsies to describe the expression landscape associated with lupus nephritis.

Cachexia is a reversible feature of inflammatory states that can become maladaptive in many diseases. A new study reveals a role for type I interferons on CD8+ T cells in mediating cachexia during viral infection.

Natural killer cells have important roles in virus and anti-cancer responses. Glimcher and colleagues demonstrate that a natural killer cell-intrinsic endoplasmic reticulum stress pathway is essential for their proper function.

Edelson and colleagues show that the transcription factor Bhlhe40 is required in a cell-intrinsic manner for the self-renewal and maintenance of large peritoneal macrophages, but not that of other tissue-resident macrophages.

Defining cell types and their activation status in rheumatoid arthritis (RA) is critical to understanding this disease. Raychaudhuri and colleagues leverage several single-cell -omics approaches to define the cellular processes and pathways in the human RA joint.

HIV-1 target cells employ a number of factors that restrict the production of viral progeny. Liang and colleagues identify the cell membrane-localized metalloprotease TRABD2A as a previously unknown restriction factor that acts at the late phase of infection to degrade HIV-1 Gag polyprotein.

RIG-I is an RNA sensor and is required for effective antiviral immunity. Cao and colleagues demonstrate that the previously undescribed long noncoding RNA Lnczc3h7a serves an essential scaffolding role in supporting productive RIG-I signaling.

Expression of the immunosuppressive cytokines IL-10 and IL-35 by tumor-infiltrating regulatory T cells drives exhaustion of intratumoral CD8+ T cells through a common pathway dependent on the transcription factor BLIMP-1.

Succinate is a signaling metabolite sensed extracellularly by SUNCR1. Fernandez-Veledo and colleagues show that activation of SUCNR1 promotes an anti-inflammatory phenotype in adipose-tissue macrophages in lean mice and people.

Comprehensive immunity requires that cells sense intracellular pathogens. In their Review, Shao and colleagues describe mechanisms for the recognition of intracellular lipopolysaccharide and its essential role in responses to Gram-negative bacteria.

Respiratory infections are the principal cause of asthma exacerbations in children. Altman and colleagues use a systems approach to describe the pathways associated with asthma exacerbations in a cohort of inner-city children.

The transcription factor PU.1 is not needed for the maintenance of neutrophil identity but is essential for the prevention of excessive tissue damage due to a prolonged immune response. PU.1 restrains the activation of neutrophils by antagonizing the AP-1 transcription factor JunB.

Fibroblastic reticular cells support lymph-node function and adaptive immunity. McGeachy and colleagues show that the cytokine IL-17 is needed to trigger metabolic changes required for the proliferation and survival of these cells in reactive lymph nodes.

Control of macrophage activation in the lungs is essential for the prevention of tissue damage. MacDonald and colleagues show that alveolar macrophages have impaired glycolysis and are hyporesponsive during type 2 inflammation in a manner controlled by the lung environment.

Neutrophils rapidly respond to bacterial and fungal infections but can cause substantial collateral tissue damage if not restrained. Rosenbauer and colleagues show that the transcription factor PU.1 serves a cell-intrinsic role to prevent over-exuberant neutrophil responses to fungal infection.

The mechanisms by which the cytokine IFN-λ regulates adaptive immune responses are poorly understood. A new study now reveals a novel IFN-λ-mediated signal-transmission system that enhances immunity after infection of the mouse respiratory tract with influenza virus.

The cytokine IL-6 controls the survival, proliferation and effector functions of lymphocytes. Jones and colleagues show that activation of CD4+ T cells leads to suppression of STAT1 activation by tyrosine phosphatases and changes the effector characteristics of memory CD4+ T cells in response to IL-6.

The skin and intestine are unique environments at the front line of the immune system. Powrie and colleagues review the distinctive adaptations acquired by regulatory T cells at these barrier surfaces.

The role of IFN-λ in adaptive immunity is not well characterized. Staeheli and colleagues show that in the lungs, IFN-λ elicits production of the cytokine TSLP from M cells and that this in turn is essential for effective adaptive immunity and control of infection with influenza virus.